Our recent studies have demonstrated that the hypocitricemic response to surgical stress is evident in rats as well as in humans. With this animal model we will investigate the underlying mechanism responsible for the decreased level of circulating citrate. A major phase of the study will involve a comparison of renal citrate utilization in control and surgical stressed (by laparotomy) animals. This study will reveal the possibility of increased renal citrate oxidation accounting for the hypocitricemia. We will also study the possible relationship of adrenal glucocorticoid (corticosterone in rats) as the mediating agent inducing the hypocitricemia. Rats will be injected with corticosterone and the changes in citrate levels determined. From such studies we will ascertain if the glucocorticoid mimics the surgical stress effect. These studies should establish if the adrenal glucocorticoid-renal activity effects on citrate regulation is an important factor in the hypocitricemic response to surgical stress.